The dimorphic yeast, Candida albicans, is the leading fungal pathogen in normal hosts and in patients with damaged immune systems. In normal hosts, disease caused by C. albicans ranges from mild, easily treated, superficial disease (e.g., thrush in newborn infants; paronychia in workers whose hands are immersed in water) to more severe, chronic or recurrent infections (e.g., candidal vaginitis). It is estimated that 5% of women of child-bearing age will suffer from recurrent candidal vaginitis (Hurley, Proc. R. Soc. Med. 70 (Suppl., 4), 1–8 (1970), and that virtually every woman will experience at least one episode during her reproductive years. Vaginitis is particularly frequent in otherwise normal females with diabetes or a history of prolonged antibiotic or oral contraceptive use. While short-term topical therapy is effective in treating individual episodes of vaginitis, such agents do not prevent recurrences. Thus, even in the normal host, infection with C. albicans can occur at epithelial surfaces, and recurrences are not prevented by presently available therapies.
In immunocompromised hosts such as cancer patients, transplant patients, post-operative surgical patients, premature newborns, or HIV-infected people, C. albicans ranks as the leading fungal pathogen. Invasion leading to systematic infection may also develop in neutropenic patients whose t-cell function is comprised. (Hostetter M K, Clinical Microbiology Reviews, January 1994, pp. 29–42.) In this population, disease ranges from aggressive local infections such as periodontitis, oral ulceration, or esophagitis in HIV-infected patients, to complex and potentially lethal infections of the bloodstream with subsequent dissemination to brain, eye, heart, liver, spleen, kidneys, or bone. Such grave prognoses require more toxic therapy, with attendant consequences from both the underlying infection and the treatment. Here again, the infection typically begins at an epithelial site, evades local defenses, and invades the bloodstream in the face of immunosuppression. Strategies to interrupt candidal adhesion therefore have broad applicability to the prevention of mild but recurrent disease in the normal host and to the reduction of substantial morbidity and mortality in the immunocompromised.
It is well recognized that C. albicans adheres to epithelial and endothelial cells in the human host, often times by recognizing proteins of the extracellular matrix called ligands. These ligands include proteins such as fibronectin, vitronectin, fibrinogen, the C3 degradation fragment iC3b, or the shorter C3 degradation fragment C3d. Because recognition of all of these proteins except C3d appears to be dependent upon the amino acid sequence ARGININE-GLYCINE-ASPARTIC ACID (or R-G-D), these candidal adhesions are thought to operate like the vertebrate integrins and are called “integrin-like proteins” or “integrin analogs.”
Vertebrate integrins are composed of two subunits: an α-subunit and a β-subunit. There are approximately 14α and 8β subunits described to date in vertebrate cells. Using monoclonal or polyclonal antibodies to vertebrate integrins, several investigators have obtained evidence for integrin-like proteins in C. albicans. 
One such protein is the protein Int1p of Candida albicans, and this protein has been observed to function as an adhesin, to participate in morphologic switching of blastospores to hyphae, and has been linked to virulence in mice. Rapid mortality ascribable to INT1/INT1 strains suggested that Int1p may have an immunomodulatory role. Pathogenesis studies using a mouse fungemia model have linked Int1p mediated adhesion and filamentation to Candida albicans virulence (Gale et al., Science 279:1355–1358, 1998), and intravenous inoculation of an int1/int1 double disruption mutant (CAG3) is associated with reduced mortality and renal inflammation compared to the wild type INT1/INT1 strain (CAF2) (see Bendel et al., Mol. Genetics and Metabolism 67:343–351, 1999).
However, mortality rates from infections from organisms such as disseminated candidas remain high despite aggressive antifungal therapy (Todischini, J. Intern Dis. 1:S37–S41, 1997), and a highly effective method of treating or preventing diseases caused by Candida albicans and other similar microorganisms expressing Int1p has yet to be obtained.